Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of the experiments with use of isoniazid and its metabolites showed that in the liver of rats isoniazid induced albuminous degeneration with stroma inflammation and hepatocyte necrosis, monoacetylhydrazine induced fatty hepatosis, acetylisoniazid induced fatty hepatosis with stroma inflammation and hepatocyte necrosis and isonicotinic acid induced granular degeneration. Piracetam proved to be efficient in fatty hepatosis. Riboxin and dibunol were efficient in hepatitis. The drugs used clinically as liver protectors, i.e. cobamamide, pyridoxal phosphate and methionine had no protective action in liver affections induced by isoniazid whereas catergen, lipamide, dipromonium and methindione even aggravated such affections.
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PMID:[Drug prophylaxis of liver lesions induced by isoniazid and its metabolites]. 274 56

The studies made showed the content of bile acids in the bile, in particular that of glycocholic one, to get moderately reduced in chronic inactive hepatitis, which fact is thought to bring about dyspeptic events showing up in the above conditions: changeable stools, periodic moderate abdominal distention, nausea and other manifestations. It has been shown that the hepatic cells functional capacity may be medically controlled. Combined use in a therapeutic complex of riboxin and ricavit resulted in normalization of the glycocholic acid content in the patients' bile. Riboxin and ricavit used separately in the therapeutic programme proved to be ineffective as a treatment option.
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PMID:[The dynamics of the glycocholic acid content of the bile in patients with chronic inactive hepatitis]. 863 Jul 89

Microsomes prepared from equine submandibular glands and incubated with tritium-labelled AcCoA incorporated acid-insoluble radioactivity in a manner dependent on time, protein, membrane integrity and AcCoA concentration, with incorporation being optimal at 37 degrees C and pH 6.6. Under the experimental conditions used a K(M) of 32.1 microM for AcCoA and a V(max) of 1.2 pmol/mg protein x min was obtained. The incorporation of acid-insoluble radioactivity was also inhibited by CoA in a competitive manner (K(i)=240 microM), as well as by para-chloromercuribenzoate, 3'-dephospho-CoA, 5'-IDP, 5'-ADP, beta-NAD and 4,4'-diisothiocyanatostilbene-2,2'-disulfonate. We demonstrate here that this incorporation of radioactivity into endogenous sialic acid is due to the action of an AcCoA:sialate-4-O-acetyltransferase [EC 2.3.1.44]. Radio thin-layer chromatography analyses of propionic acid-released sialic acids showed that the incorporation of radioactivity correlated with the formation of a radiolabelled species that co-migrated with authentic Neu4,5Ac2. Saponification experiments using NaOH, mouse hepatitis virus strain S and Influenza C/JJ/50 virus also showed that the transfer of [3H]acetyl groups from [3H]AcCoA to endogenous sialic acid acceptors was occurring exclusively at carbon 4 of the pyranose ring.
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PMID:Characterisation of the enzymatic 4-O-acetylation of sialic acids in microsomes from equine submandibular glands. 1151 9